Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages
Under serum‐free conditions the β‐glucan receptor of mouse macrophages mediates phagocytosis of β‐l,3‐D‐glucan‐coated microbeads (diameter 2 μm). IFN‐γ increases the phagocytic function of the β‐glucan receptor in a dose‐dependent manner, giving the plateau level at 100 U/ml. Maximum activity appear...
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Veröffentlicht in: | Scandinavian journal of immunology 1993-05, Vol.37 (5), p.587-592 |
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description | Under serum‐free conditions the β‐glucan receptor of mouse macrophages mediates phagocytosis of β‐l,3‐D‐glucan‐coated microbeads (diameter 2 μm). IFN‐γ increases the phagocytic function of the β‐glucan receptor in a dose‐dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN‐γ to the cells. The effect disappears within 24 h. The effect of IFN‐γ may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis.
IL‐1 also increases the phagocytic function of the β‐glucan receptor giving a dose‐dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL‐I to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β‐glucan receptor, but TNF together with IL‐1 prolongs the effect of IL‐1.
PGE2 reduces the phagocytic function of the β‐glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time‐course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells. |
doi_str_mv | 10.1111/j.1365-3083.1993.tb02576.x |
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IL‐1 also increases the phagocytic function of the β‐glucan receptor giving a dose‐dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL‐I to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β‐glucan receptor, but TNF together with IL‐1 prolongs the effect of IL‐1.
PGE2 reduces the phagocytic function of the β‐glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time‐course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells.</description><identifier>ISSN: 0300-9475</identifier><identifier>EISSN: 1365-3083</identifier><identifier>DOI: 10.1111/j.1365-3083.1993.tb02576.x</identifier><identifier>PMID: 8387227</identifier><identifier>CODEN: SJIMAX</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Analysis of the immune response. Humoral and cellular immunity ; Animals ; Biological and medical sciences ; Cells, Cultured ; Cytokines - pharmacology ; Dinoprostone - pharmacology ; Dose-Response Relationship, Immunologic ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Glucans - metabolism ; Immunobiology ; Interferon-gamma - pharmacology ; Interleukin-1 - pharmacology ; Macrophages - drug effects ; Macrophages - immunology ; Mice ; Microspheres ; Miscellaneous ; Phagocytosis - drug effects ; Phagocytosis - immunology ; Receptors, Cell Surface - drug effects ; Receptors, Cell Surface - immunology ; Receptors, Complement - drug effects ; Receptors, Complement - immunology ; Receptors, Immunologic ; Regulatory factors and their cellular receptors ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Scandinavian journal of immunology, 1993-05, Vol.37 (5), p.587-592</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3987-d63a30e33d240f06685f00e08b492b119c11bc92ff38985b0fc78edfa97ebedc3</citedby><cites>FETCH-LOGICAL-c3987-d63a30e33d240f06685f00e08b492b119c11bc92ff38985b0fc78edfa97ebedc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-3083.1993.tb02576.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-3083.1993.tb02576.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4780468$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8387227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KONOPSKI, Z.</creatorcontrib><creatorcontrib>SELJELID, R.</creatorcontrib><creatorcontrib>ESKELAND, T.</creatorcontrib><title>Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages</title><title>Scandinavian journal of immunology</title><addtitle>Scand J Immunol</addtitle><description>Under serum‐free conditions the β‐glucan receptor of mouse macrophages mediates phagocytosis of β‐l,3‐D‐glucan‐coated microbeads (diameter 2 μm). IFN‐γ increases the phagocytic function of the β‐glucan receptor in a dose‐dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN‐γ to the cells. The effect disappears within 24 h. The effect of IFN‐γ may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis.
IL‐1 also increases the phagocytic function of the β‐glucan receptor giving a dose‐dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL‐I to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β‐glucan receptor, but TNF together with IL‐1 prolongs the effect of IL‐1.
PGE2 reduces the phagocytic function of the β‐glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time‐course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells.</description><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Cytokines - pharmacology</subject><subject>Dinoprostone - pharmacology</subject><subject>Dose-Response Relationship, Immunologic</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Glucans - metabolism</subject><subject>Immunobiology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Interleukin-1 - pharmacology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - immunology</subject><subject>Mice</subject><subject>Microspheres</subject><subject>Miscellaneous</subject><subject>Phagocytosis - drug effects</subject><subject>Phagocytosis - immunology</subject><subject>Receptors, Cell Surface - drug effects</subject><subject>Receptors, Cell Surface - immunology</subject><subject>Receptors, Complement - drug effects</subject><subject>Receptors, Complement - immunology</subject><subject>Receptors, Immunologic</subject><subject>Regulatory factors and their cellular receptors</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0300-9475</issn><issn>1365-3083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkE9u1DAUh60KVIbSI1SyKtRdwrOdxDYLpGrUDkWtqPizreU4zzTTTDyNE9HZcQTOwkE4BCchw0Szx5u3-H2_56ePkFMGKRvfm2XKRJEnApRImdYi7UvguSzSpwMy20fPyAwEQKIzmb8gL2NcAjDBpTgkh0ooybmckbv5pg8PdYuR2rait4sLTm9CNTS2R9rfI729t9-C2_S1o5dD6_o6tDT4f9HvX39-_Fw0g7Mt_YQO133oaN3SG-u6sB57GF-R5942EY-neUS-Xl58mb9Prj8urubn14kTWsmkKoQVgEJUPAMPRaFyD4CgykzzkjHtGCud5t4LpVVegndSYeWtllhi5cQROdvtXXfhccDYm1UdHTaNbTEM0chcMp6DHMG3O3A8McYOvVl39cp2G8PAbOWapdkaNFuDZivXTHLN01g-mX4ZyhVW--pkc8xfT7mNzja-s62r4x7LpIKsUCP2bod9rxvc_McB5vOHq1xJ8RcKz5gV</recordid><startdate>199305</startdate><enddate>199305</enddate><creator>KONOPSKI, Z.</creator><creator>SELJELID, R.</creator><creator>ESKELAND, T.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199305</creationdate><title>Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages</title><author>KONOPSKI, Z. ; SELJELID, R. ; ESKELAND, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3987-d63a30e33d240f06685f00e08b492b119c11bc92ff38985b0fc78edfa97ebedc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Cytokines - pharmacology</topic><topic>Dinoprostone - pharmacology</topic><topic>Dose-Response Relationship, Immunologic</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Glucans - metabolism</topic><topic>Immunobiology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Interleukin-1 - pharmacology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - immunology</topic><topic>Mice</topic><topic>Microspheres</topic><topic>Miscellaneous</topic><topic>Phagocytosis - drug effects</topic><topic>Phagocytosis - immunology</topic><topic>Receptors, Cell Surface - drug effects</topic><topic>Receptors, Cell Surface - immunology</topic><topic>Receptors, Complement - drug effects</topic><topic>Receptors, Complement - immunology</topic><topic>Receptors, Immunologic</topic><topic>Regulatory factors and their cellular receptors</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KONOPSKI, Z.</creatorcontrib><creatorcontrib>SELJELID, R.</creatorcontrib><creatorcontrib>ESKELAND, T.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Scandinavian journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KONOPSKI, Z.</au><au>SELJELID, R.</au><au>ESKELAND, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages</atitle><jtitle>Scandinavian journal of immunology</jtitle><addtitle>Scand J Immunol</addtitle><date>1993-05</date><risdate>1993</risdate><volume>37</volume><issue>5</issue><spage>587</spage><epage>592</epage><pages>587-592</pages><issn>0300-9475</issn><eissn>1365-3083</eissn><coden>SJIMAX</coden><abstract>Under serum‐free conditions the β‐glucan receptor of mouse macrophages mediates phagocytosis of β‐l,3‐D‐glucan‐coated microbeads (diameter 2 μm). IFN‐γ increases the phagocytic function of the β‐glucan receptor in a dose‐dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN‐γ to the cells. The effect disappears within 24 h. The effect of IFN‐γ may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis.
IL‐1 also increases the phagocytic function of the β‐glucan receptor giving a dose‐dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL‐I to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β‐glucan receptor, but TNF together with IL‐1 prolongs the effect of IL‐1.
PGE2 reduces the phagocytic function of the β‐glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time‐course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>8387227</pmid><doi>10.1111/j.1365-3083.1993.tb02576.x</doi><tpages>6</tpages></addata></record> |
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subjects | Analysis of the immune response. Humoral and cellular immunity Animals Biological and medical sciences Cells, Cultured Cytokines - pharmacology Dinoprostone - pharmacology Dose-Response Relationship, Immunologic Female Fundamental and applied biological sciences. Psychology Fundamental immunology Glucans - metabolism Immunobiology Interferon-gamma - pharmacology Interleukin-1 - pharmacology Macrophages - drug effects Macrophages - immunology Mice Microspheres Miscellaneous Phagocytosis - drug effects Phagocytosis - immunology Receptors, Cell Surface - drug effects Receptors, Cell Surface - immunology Receptors, Complement - drug effects Receptors, Complement - immunology Receptors, Immunologic Regulatory factors and their cellular receptors Tumor Necrosis Factor-alpha - pharmacology |
title | Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages |
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